Our group has previously shown that migraineurs, as opposed to individuals with other headaches, are more likely to have headache during the bright arctic summer than during the polar night season. We set out to investigate the impact of seasonal light exposure in migraine with and without aura. We performed a questionnaire-based study of 169 female volunteer migraineurs in an arctic area where light conditions during summer and winter seasons are extreme. We included 98 patients with migraine with aura (MA) and 71 with migraine without aura (MoA). One hundred and seven patients (63%) reported seasonal variation in migraine attack frequency. Close to half (47%) of patients with aura, but only 17% of patients without aura, reported more frequent attacks during the light season (P < 0.001). Patients with MA reported interictal light hypersensitivity and light exposure as an attack precipitating factor significantly more often than individuals with MoA. They also reported significantly more frequent use of sunglasses to prevent attacks. We found no significant differences between MA and MoA as regards sleep disturbances, use of oral contraceptives, impact of headache or circadian variations. Seasonal periodicity of migraine in an arctic population with more frequent attacks during the light season is a convincing phenomenon in MA but not in MoA. The amount of light exposure seems to be pivotal to this variation.

Migraine is a complex brain disorder where several neuronal pathways and neurotransmitters are involved in the pathophysiology. To search for a specific anatomical or physiological defect in migraine may be futile, but the hypothalamus, with its widespread connections with other parts of the central nervous system and its paramount control of the hypophysis and the autonomic nervous system, is a suspected locus in quo. Several lines of evidence support involvement of this small brain structure in migraine. However, whether it plays a major or minor role is unclear. The most convincing support for a pivotal role so far is the activation of the hypothalamus shown by positron emission tomography (PET) scanning during spontaneous migraine attacks. A well-known theory is that the joint effect of several triggers may cause temporary hypothalamic dysfunction, resulting in a migraine attack. If PET scanning had consistently confirmed hypothalamic activation prior to migraine headache, this hypothesis would have been supported. However, such evidence has not been provided, and the role of the hypothalamus in migraine remains puzzling. This review summarizes and discusses some of the clues.

It is a general belief that migraine attacks are prone to occur on days off. Only a few studies, however, have addressed this issue. The objective of this study was to investigate the periodicity of migraine with respect to weekly (circaseptan) variations. Eighty-nine females of fertile age who had participated in a previous questionnaire-based study volunteered to record in detail every migraine attack for 12 consecutive months. Eighty-four patients completed recordings for a mean of 311 days (s.d. = 95.9, range 30-365). A total of 2314 attacks were recorded. Migraine occurrence was almost equally distributed during the week, except on Sundays, when there were significantly fewer attacks (t = -4.42, d.f. = 83, P < 0.001). A Mantel-Haenszel estimate of the relative risk of having an attack on a holiday vs. another day, not Sundays included, was 0.64 (95% CI 0.49-0.85). Our study suggests that days off protect against migraine.

The aim of the study was to study seasonal variation in migraine headache in a group of women with menstrually-related migraine (MRM) compared with non-menstrual migraine. Via newspaper advertisement, women with migraine living in North Norway were invited. The patients were included by questionnaire and telephone interview. We prospectively recorded migraine attacks from a 12-month headache diary performed by a group of 62 women with a mean age of 36.0 years (range 16-46 years), who fulfilled the criteria of migraine without aura. Of these, 29 had MRM and 33 non-menstrual migraine. Mean ratio between number of attacks in the light arctic season (May-June-July) divided with total number of migraine attacks during 12 months was 0.24 (9.4/38.4) in the group of MRM compared with 0.25 (5.6/22.1) in others (confidence interval -4.2, 6.3, P = 0.84). Nor were there more migraine attacks in the dark season in an arctic area (November-December-January) in any group. We found a higher migraine attack rate in those with MRM, but no indication of more or less frequency of attacks during the bright arctic season. These findings support the assumption that MRM and seasonal variation of migraine are due to different mechanisms.